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Exp Neurol
2012[May]; 235
(1
): 133-41
PMID22116043
show ga
Whether dramatic or modest, recovery of neurological function after spinal cord
injury (SCI) is greatly due to neuroplasticity--the process by which the nervous
system responds to injury by establishing new synaptic connections or by altering
the strength of existing synapses. However, the same neuroplasticity that allows
locomotor function to recover also produces negative consequences such as pain
and dysfunction of organs controlled by the autonomic nervous system. In this
review we focus specifically on structural neuroplasticity (the growth of new
synaptic connections) after SCI and on the consequent development of pain and
autonomic dysreflexia, a condition of episodic hypertension. Neuroplasticity
after SCI is stimulated by the deafferentation of spinal neurons below the lesion
and by the expression of growth-promoting neurotrophins such as nerve growth
factor (NGF). A broad range of therapeutic strategies that affect neuroplasticity
is being developed for the treatment of SCI. At one end of the spectrum are
therapeutic strategies that directly or indirectly increase NGF in the injured
spinal cord, and have the most robust effects on neuroplasticity. At the other
end of the spectrum are neuroprotective strategies focused on supporting and
rescuing uninjured, or partially injured, axons; these might limit the
deafferentation stimulus for neuroplasticity. In the middle of this spectrum are
strategies that block axon growth inhibitors without necessarily providing a
growth stimulus. The literature supports the view that the negative consequences
of neuroplasticity develop more commonly with therapies that directly stimulate
nerve growth than they develop in the untreated injured cord. Compared to these
conditions, neuroplasticity with negative outcomes is less prevalent after
treatments that that neutralize axon growth inhibitors, and least apparent after
strategies that promote neuroprotection.
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